Skip to content
akaturk Academic measurement

Article detail · 2007

The Effect of Intrahippocampal Beta Amyloid 1 42 Peptide Injection on Oxidant and Antioxidant Status in Rat Brain

YÖKSİS OpenAlex SJR Q1 JCR Q1 Citations 42 Percentile 70.8% FWCI 0.82
Year
2007
Type
article

Data source split

  • YÖKSİS YÖKSİS article record
  • YÖKSİS venue Annals of the New York Academy of Sciences
  • Catalog match (ISSN) Annals of the New York Academy of Sciences
  • OpenAlex OpenAlex enrichment (abstract, citations, topics)

Abstract

English (OpenAlex)

In some animal models, cognitive impairment and neurodegenerative disorders that mimic Alzheimer's disease (AD) can be reproduced by intracerebral or intracerebroventricular administration of peptide (Abeta) beta amyloid. Evidence suggests that oxidative stresses are involved in the mechanism of Abeta-induced neurotoxicity and AD pathogenesis. Exposure to Abeta increases lipid peroxidation, protein oxidation, and the formation of hydrogen peroxide in cultured cells. Nitric oxide (NO) has significant physiological roles in the central nervous system and also it can be implicated in neurodegenerative diseases because of its free radical properties. The purpose of this study is to search the effects of intrahippocampal Abeta (1-42) injection on malondialdehyde (MDA), glutathione (GSH), and nitrite plus nitrate (NOx) levels in temporal cortex and basal forebrain in rats. In this study, male adult Wistar albino rats were divided into two groups. Abeta (1-42) peptide (10 mug/2 muL) was administered bilaterally as a single injection into the hippocampal fissure by a Hamilton microsyringe. Distilled water was administered to the control group by using the same procedure. Ten days after the Abeta (1-42) injection, the rats were decapitated and brains were rapidly removed. MDA, GSH, and NOx levels were analyzed spectrophotometrically in temporal cortex and basal forebrain. MDA levels and NOx were increased 10 days after the injection of Abeta (1-42) in temporal cortex and basal forebrain, but no statistical significance was found compared to control group. However, GSH levels were significantly higher in temporal cortex and basal forebrain in the Abeta (1-42)-injected group than the control group (P < 0.05). In conclusion, increased levels of GSH in temporal cortex and basal forebrain after the intrahippocampal Abeta (1-42) injection show that a protective mechanism might develop due to oxidative stress.

Topics

  • Alzheimer's disease research and treatments
  • Biochemical effects in animals
  • Neurological Disease Mechanisms and Treatments

Primary topic Alzheimer's disease research and treatments

Authors

  1. FERİHAN ÇETİN İSTANBUL MEDENİYET ÜNİVERSİTESİ
  2. SİBEL DİNCER